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Biomedical subjects

D A Feinfeld

Publications and source records attributed to D A Feinfeld.

52 records · Page 3Linked to original sources
PubMed1980

An outbreak of Salmonella enteritis and septicemia in a population of uremic patients. A review of four cases, including infection of an arteriovenous fistula.

An outbreak of enteritis and septicemia caused by Salmonella enteritidis occurred in a population of uremic patients treated in a nephrology unit. In one of the patients, an arteriovenous fistula was infected by this organism. The source of the outbreak was traced to the refrigerator and sink in the unit. This degree of morbidity and mortality far exceeds that previously reported in infections with nontyphoid Salmonella sp and is presumbly related to the decreased immune response seen in uremia.

Adult↗
PubMed1979

Non-A, non-B hepatitis: a new syndrome in uraemic patients.

One hundred patients on chronic haemodialysis were studied prospectively over one year for evidence of hepatitis and of infection with hepatitis A or B virus. Five patients developed transient elevations of SGPT, accompanied by a consistent pattern of clinical manifestations, including low-grade fever, anorexia, nausea, hepatomegaly, and hypotension during dialysis. None of these patients had a positive test for A or B virus infection. Non-A non-B hepatitis appears to cause a specific syndrome in uraemic patients, and its transmission in a dialysis unit seems unrelated to blood transfusions.

Aged↗
PubMed1979

Ligandinuria: an indication of tubular cell necrosis.

Ligandinuria is a useful index of acute tubular injury. Ligandin probably enters the urine at the time of initial necrosis and should be looked for soon after the toxic or ischemic event. Periodic examination of perfusates for this substance might yield useful information about techniques for storage of cadaver kidneys.

Animals↗
PubMed1978

Search for the uremic toxin. Decreased motor-nerve conduction velocity and elevated parathyroid hormone in uremia.

In a retrospective analysis to determine whether secondary hyperparathyroidism in uremia has a role in uremic peripheral neuropathy, we simultaneously measured motor-nerve conduction velocity and serum parathormone level in 42 uremic patients. We compared age-matched groups of nondiabetic uremic patients, divided into three groups according to serum parathyroid hormone, for degree of impairment of motor-nerve conduction velocity, and 12 diabetic patients with uremia. The group with highest levels had a significantly (P less than 0.01) lower conduction velocity (25.3 +/- 4.9 m per second) than the group with normal or slightly elevated parathyroid hormone, who had only mild depression of nerve conduction (45.1 +/- 1.3 m per second). Mean serum calcium and creatinine were not significantly different between groups. Nerve conduction velocity was similarly depressed in 17 patients on additional dialysis studied prospectively and divided into groups according to parathyroid hormone levels. These results suggest a relation between high parathormone levels and uremic neuropathy and implicate parathyroid hormone as a uremic toxin.

Adult↗
PubMed1978

Ligandin in perfusates from transplanted kidneys: a test for tubular necrosis.

Ligandin, an intracellular organic anion-binding protein, having glutathione-S-transferase activity, was detected in concentrated perfusing solutions from 8 of 13 kidneys preserved for homotransplantation. The presence of ligandin in the perfusate correlated well with oliguric acute renal failure following transplantation. Testing the perfusate for ligandin may be useful in predicting tubular damage in renal transplants.

Acute Kidney Injury↗
PubMed1977

Ligandinuria in nephrotoxic acute tubular necrosis.

Ligandin (GSH-S-transferase B), an abundant intracellular soluble protein in rat proximal tubules, hepatocytes, and small intestinal mucosal cells, is believed to be a component of an organic anion transport system. Its presence in urine was determined immunologically and catalytically in adult, female, Sprague-Dawley rats that were given mercuric chloride or potassium dichromate. These nephrotoxic agents produce severe renal failure, with epithelial necrosis in the proximal tubule. Mercuric chloride perferentially injures the terminal part of the proximal tubule, while potassium dichromate damages more proximal segments. Ligandinuria was consistently detected immunologically and catalytically from 6 to 24 hr following injection of mercuric chloride. Potassium dichromate administration did not result in immunologically detectable liganduria; however, GSH-S-transferase activity, which provides a more sensitive assay, was frequently detected. The findings are consistent with immunofluorescent localization of ligandin in the proximal tubule. Immunologic or enzymatic measurement of ligandin in urine may provide a sensitive index of acute injury to the proximal tubule.

Acute Kidney Injury↗
PubMed1977

Lupus nephritis in a neuronal storage disease.

Systemic lupus erythematosus (SLE) with glomerulonephritis occurred in a patient with a long-standing neuronal storage disease and myoclonus. Intravenously administered diazepam was useful in controlling the myoclonus to permit a renal biopsy. The exact relationship between the patient's underlying illness and the development of SLE remains unknown.

Diazepam↗
PubMed1976

Enzymatic evidence of renal tubular damage following renal angiography.

Ligandin, a glutathione (GSH) transferase, is a protein found in proximal tubular cells as well as in other tissues. It does not occur in the urine of normal subjects; however, its presence has been detected in the urine of some patients who have undergone renal angiography. This finding suggests renal tubular cell damage due to the procedure.

Acute Kidney Injury↗
PubMedDate not supplied

A microradiographic study of nephrons in mercuric chloride-induced acute renal failure in the rabbit.

Microradiography of nephrons was performed on glutaraldehyde-perfusion-fixed kidneys from rabbits injected with mercuric chloride. Kidneys were studied at intervals after injection of the toxin and compared with controls. All mercury-injected animals developed acute renal failure, determined by a rise in serum creatinine. At 6 hours, small filling defects were seen in proximal straight tubules, arising from the wall, and by 24 hours, widespread tubular obstruction was noted. By 12 hours, dilatation of Bowman's space and compression of the glomerular tuft were seen. At 18 hours, preferential channels in the glomerular capillary loops were found, and by 24 hours, there was paraglomerular shunting. No changes were noted in afferent or efferent arterioles. These findings may be related to the decreased glomerular filtration rate seen in acute nephrotoxic renal failure and suggest a role for tubular obstruction in the pathophysiology of this disorder.

Acute Kidney Injury↗
PubMedDate not supplied

A simple estimate of the effect of the serum albumin level on the anion Gap.

BACKGROUND: The serum anion gap (serum [Na(+)]-Cl(-)]-[CO(2)]) is still the first-line approach to metabolic acidosis. However, while it is generally acknowledged that hypoalbuminemia mandates a downward adjustment of the expected anion gap, a specific correction factor for the anion gap in the face of low serum albumin has never been demonstrated. METHODS: We reviewed initial laboratory data from 432 consecutive patients admitted or transferred to the medical intensive care unit at Nassau County Medical Center over a 6-month period and correlated the serum albumin with the anion gap and the serum [tCO(2)] using multivariate analysis. We looked at the anion gap as a function of delta (albumin), the difference between normal and actual serum albumin, defined as 4.0 - measured serum albumin g/dl. We also assessed [tCO(2)] as an independent variable. RESULTS: For patients with normal or high serum tCO(2), the ratio of change in anion gap (delta anion gap) to delta (albumin) was 1.46 and 1.45, respectively. For patients with serum tCO(2) <22 mEq/l this ratio was 1.89. In the latter group, anion gap was best predicted taking both delta (albumin) and serum tCO(2) into account: anion gap = 36.2 - serum tCO(2) - 2.3 x delta (albumin) (r = 0.71, p < 0.0001). CONCLUSION: For intensive care patients with normal or high serum tCO(2) (>21 mEq/l) a simple bedside adjustment of the anion gap by subtracting 1.5 times the difference between measured serum albumin and the 'normal' level of 4.0 g/dl gives a close estimate of the actual anion gap. For intensive care patients with serum tCO(2) <22 mEq/l, correction of the anion gap is well predicted by adding about twice the Delta (albumin) to the calculated gap.

Acid-Base Equilibrium↗
PubMedDate not supplied

Life-threatening hyperkalemia after intravenous labetolol injection for hypertensive emergency in a hemodialysis patient.

Intravenous labetolol, a nonselective alpha- and beta-blocking drug, is commonly used to treat severe hypertension. Nonselective beta-blockers can cause hyperkalemia, especially in patients with renal failure. One series reported 3 renal transplant patients who had hyperkalemia after labetolol infusion, but none of these patients developed any serious complication. We report a case of life-threatening hyperkalemia (serum [K+] 9.9 mEq/l) with ventricular tachycardia and hypotension in a patient on maintenance hemodialysis who received labetolol for a hypertensive emergency. Physicians should be aware of this potentially lethal complication, which is easily preventable.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

A prospective study of urinary ligandin in patients at risk of renal tubular injury.

The urinary excretion of ligandin, a proximal tubular enzyme and binding protein, was measured by radioimmunoassay in eight normals, six patients receiving radiocontrast media, and six patients in a critical care unit who were considered at high risk for acute renal failure. Ligandinuria was found to occur normally at rates under 5 micrograms/hr. In the patients receiving radiocontrast media, abnormal rates of ligandinuria were found in four patients. In 102 ligandin measurements in the critically ill patients, rates of ligandinuria exceeded normal only once (after contrast media exposure) despite 13 identifiable episodes of potentially nephrotoxic circumstances and two episodes of acute renal failure. Ligandinuria appears more sensitive as a marker for tubular injury from contrast media than from other renal insults.

Acute Kidney Injury↗